earticle

영어

UV irradiation on the skin induces photoaging. It is characterized by thickening, keratinocyte hyperproliferation, coarse wrinkles, laxity and roughness. NF-κB is activated upon UV irradiation and plays a key role in signaling pathway leading to inflammation cascade. It stimulates expression of pro-inflammatory cytokines such as TNF-α, IL-1α and COX-2. In addition, activation of NF-κB up-regulates the expression of MMP-1 and consequently degrades the collagen in dermis, which is a major cause in photoaging process. In this study, the effect of a NF-κB specific inhibitor tripeptide on the UVB-induced photoaging and inflammation was analyzed in vitro and in vivo. A NF-κB specific inhibitor tripeptide was synthesized based on the sequence of DNA binding site of the subunit p65 of NF-κB. The effect of NF-κB inhibitor peptide on anti-photoaging was measured by western blotting, RT-PCR, ELISA, and immuno staining respectively. We found that treatment with NF-κB inhibitor peptide significantly decreased UV-induced TNF-α, IL-1α, COX-2 and MMP-1 expression and markedly increased the level of typeⅠ procollagen. Also, the topical application of NF-κB inhibitor peptide significantly inhibited the increase in epidermal thickness of hairless mice. These results indicate that NF-κB inhibitor peptide could prevent UV-induced skin inflammation and therefore could be used as a novel cosmeceutical for anti-photoaging.